Molecular Mechanisms Underlying Yatein-Induced Cell-Cycle Arrest and Microtubule Destabilization in Human Lung Adenocarcinoma Cells
- Cancers (Basel). 2019 Sep 17;11(9):1384. doi: 10.3390/cancers11091384.
- 1. Department of Forestry, National Chung Hsing University, Taichung 402, Taiwan. [email protected].
- 2. Agricultural Biotechnology Research Center, Academia Sinica, Taipei 115, Taiwan. [email protected].
- 3. Institute of Biomedical Science, National Chung Hsing University, Taichung 402, Taiwan. [email protected].
- 4. Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei 110, Taiwan. [email protected].
- 5. Nutrition Research Center, Taipei Medical University Hospital, Taipei 110, Taiwan. [email protected].
- 6. Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei 116, Taiwan. [email protected].
- 7. Department of Forestry, National Chung Hsing University, Taichung 402, Taiwan. [email protected].
Yatein is an antitumor agent isolated from Calocedrus formosana Florin leaves extract. In our previous study, we found that yatein inhibited the growth of human lung adenocarcinoma A549 and CL1-5 cells by inducing intrinsic and extrinsic apoptotic pathways. To further uncover the effects and mechanisms of yatein-induced inhibition on A549 and CL1-5 cell growth, we evaluated yatein-mediated antitumor activity in vivo and the regulatory effects of yatein on cell-cycle progression and microtubule dynamics. Flow cytometry and western blotting revealed that yatein induces G2/M arrest in A549 and CL1-5 cells. Yatein also destabilized microtubules and interfered with microtubule dynamics in the two cell lines. Furthermore, we evaluated the antitumor activity of yatein in vivo using a xenograft mouse model and found that yatein treatment altered cyclin B/Cdc2 complex expression and significantly inhibited tumor growth. Taken together, our results suggested that yatein effectively inhibited the growth of A549 and CL1-5 cells possibly by disrupting cell-cycle progression and microtubule dynamics.